Non-steroidal anti-inflammatory medication, or NSAIDs, are widely used as a pain reliever, to reduce fevers and to lower inflammation. They are readily available in any household in over-the-counter form, such as aspirin or ibuprofen for example.
This is a great research piece and a very important one especially for the world of sports, where the use of NSAIDs is very prevalent. K (aka my husband Konstantin, Coach K) forwarded it to me this morning. I would like to make sure I have it for easy future reference, so I will paste the text here as well as provide the link to the actual paper. Links often get broken and I like to have the material accessible for me and for our readers.
The reason this research caught K’s attention is that he has suffered from chronic inflammation for years. It stems from sports injuries, overuse after years of training, and not sufficiently recovering. Of course, now we understand that an inflammatory diet full of processed foods, toxic oils, high levels of sugar, and bad quality fats, as well as the inability to effectively manage stress among other things, were some of the main epigenetic factors he was exposing his system to over the years. Hence his complete dependency on NSAIDs for years. He was only able to get off of them after fully embracing an anti-inflammatory diet, Bulletproof lifestyle, Deep Nutrition principles, stress management and finally developing his 108Strong Fitness system.
The latest scientific research shows that these painkillers can have negative side effects and increase the danger of heart attacks, strokes, and kidney or heart failure. In our household, these are treated as serious medications and we no longer keep them on a kitchen counter for a casual everyday-headache-or-any-other-pain-relief go-to option.
So here is the article, unedited:
“Non-steroidal anti-inflammatory drugs, or NSAIDs, are commonly used as inflammation blockers worldwide. However, recent clinical data show these painkillers can have serious side effects that create some risk of heart attacks, strokes, and kidney or heart failure.
Attention has focused on how NSAIDs may cause dysfunction of the immune system, including disrupting the normal immune response involved after heart injury. This normal response has two stages — the acute phase, where leukocytes from the spleen migrate to the heart’s left ventricle to clear out dead heart-muscle cells and form scar tissue, followed by a resolving phase to dampen the acute inflammation.
University of Alabama at Birmingham researchers, led by Ganesh Halade, Ph.D., an assistant professor in the UAB Department of Medicine’s Division of Cardiovascular Disease, have now studied such dysfunction associated with the NSAID carprofen. In a study published in the Journal of Leukocyte Biology, they found that sub-acute pretreatment with carprofen before experimental heart attack in mice impaired resolution of acute inflammation following cardiac injury.
They focused on three aspects of the inflammation resolution axis — cardiac function, leukocyte profiling and inflammation-resolution markers.
They found that, after heart attack, the carprofen-pretreated mice had a greatly intensified amount of the CD47 cell-surface marker in the left ventricle and the spleen. The CD47 marker is a “don’t eat me” signal, and the increased CD47 was found to be on neutrophil cells, which are involved in acute inflammation after heart injury. Thus, the amplified CD47 on neutrophils resisted clearance of the neutrophils and developed a non-resolving inflammation.
The UAB researchers also found that carprofen treatment before heart attacks pre-activated neutrophils in the spleen to make them more inflammatory, and it also activated pro-inflammatory macrophages. This helped trigger the swarming of activated neutrophils from the spleen to the left ventricle after the heart attack. At the same time, reparative leukocytes in the left ventricle were compromised.
Carprofen pre-treatment failed to limit expression of the enzymes cyclooxygenase-1 and cyclooxygenase-2, further dysregulating the production of resolving lipid mediators, which created a deficit in the resolution of inflammation in the injured heart.
Furthermore, the carprofen pretreatment led to an imbalance of inflammatory and reparative cytokines after cardiac injury, and this expanded the inflammatory phase in the injured heart.
Co-authors with Halade of the study, “Subacute treatment of carprofen facilitates splenocardiac resolution deficit in cardiac injury,” are Vasundhara Kain, Griffin M. Wright and Jeevan Kumar Jaddapalli, Division of Cardiovascular Disease, UAB Department of Medicine.
Support came from National Institutes of Health grants AT006704 and HL132989, a University of Alabama at Birmingham Pittman Scholar Award, and American Heart Association postdoctoral fellowship POST31000008.”
To your health,